Relationships between mucosal microbial taxa and the expression of inflammatory genes in Crohn's Disease
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In recent years there have been major advances in our understanding of the mechanisms that are involved in the recognition of microbes and subsequent activation of host immune defenses. Several classes of membrane-bound and cytosolic pattern recognition receptors (PRRs) have been identified and partially characterized. These include the Toll-like receptors (TLRs), NOD-like receptors (NLRs) and RIG-I-like receptors (RLRs). Activation of PRRs leads to the production of a large array of pro-inflammatory and anti-microbial molecules that are critical for the elimination of invading pathogens, and activation of adaptive immune responses. A class of cytosolic PRRs is involved in the assembly of the inflammasome, a molecular platform that mediates activation of caspase-1 and secretion of mature IL-1beta and IL-18. Importantly, activation of the inflammasome is also induced by non-microbial mechanisms including endogenous molecules involved in the pathogenesis of metabolic and inflammatory diseases. In addition, there is evidence that autophagy, a cellular process that mediates recycling of intracellular components, is involved in microbial recognition and plays a key role in host defense. The initial sensing of microbes often occurs at mucosal surfaces, but the interplay between recognition of commensal vs. pathogenic microbes on the host immune system is only beginning to be uncovered. The goal of the Keystone Symposia meeting on Innate Immunity: Sensing the Microbes and Damage Signals is to gather scientists working on innate immunity to discuss cutting edge research on the mechanisms that regulate the activation of the immune system by microbes as well as by endogenous damage signals, and to integrate such knowledge in the context of inflammation, homeostasis, host defense, and disease. Opportunities for interdisciplinary interactions will be significantly enhanced by the concurrent meeting on The Microbiome, which will share a keynote address and three plenary sessions with this meeting.
The current prevailing hypothesis for the pathogenesis of Crohn's disease (CD) states that it Involves an Inappropriate and ongoing activation of the mucosal Immune system drlvan by the Intestinal mlcroblola In genelfcally predisposed Individuals'. Our aim was to evaluate evidence that the composilion of the gut microblota plays a role In unbalancing of Immune system.